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Hepatocellular carcinoma (HCC) are themost common primary liver tumor in male dogs(The Merck Veterinary Manual 2010) and it isnot uncommon in sniffer dog. These neoplasmstypically affect younger dogs, more than two-thirds of the dogs are less than 10 years old(Patnaik et al. 2005). It occurs frequently inmammalian hosts including human (Bertino1996). Several workers were reported hepato-cellular carcinoma in different canine species(Patnaik et al. 1980, Evans 1987, Liptak etal. 2004, Sterczer et al. 2011).

A carcass of sniffer Labrador dog ofCentral Industrial Security Force, KolkataPort Trust, aged about three years and sixmonths was brought to Disease InvestigationLaboratory, Institute of Animal Health &Veterinary Biologicals, Kolkata, India forpostmortem examination to ascertain thecause of death. The dog was suffering inchronic hepatic disorders for last few monthswith the history of anorexia, lethargy,weakness, inactivity, apathy, weight loss,

polydipsia, vomition, abdominal pain andascites. It was finally unfit for trainingprogramme and duty before death.

Haematological and biochemicalparameters primarily revealed Total LeucocyticCount (TLC) 6,800 cu. mm, DifferentialLeucocytic Count (DLC) ( Neutrophil 84%,Lymphocyte 13%, Monocyte 1%, Eosinophil2%, Basophil 0% ), Haemoglobin 10.4 gm%,Serum urea 39.80 mg/dl, Blood Urea Nitrogen(BUN) 19.00 mg/dl, Serum creatinine 1.55mg/dl, SGPT/ALT 83.10 u/l, SGPT/ASL84.60 u/l, Serum potassium 4.60 mcg/l, TotalSerum protein 6.80 gm% ( Albumin 3.40gm%, Globulin 3.40 gm%, Albumin Globulinratio 1 : 1 ). The Thyroid function test byChemiluminescence assay (CLIA) showedTotal triiodothyroxin (T

3) 1.44 ng/ml, Total

thyroxin (T4) 10.87 µg/dl, Thyroid stimulating

hormone (TSH) 0.34 ng/ml. Examination ofaspirated peritoneal fluid revealed presenceof blood cells predominantly lymphocyteswith nucleated total cell 780 / cu. mm, Sugar

Short Communication

HEPATOCELLULAR CARCINOMA IN A DOG - A CASEREPORT

Shivaji Bhattacharya, B. Dutta, J. Mukherjee, G. Chakraborty and Malay Mitra

Institute of Animal Health & Veterinary Biologicals,

37, Belgachia Road, Kolkata - 700037, West Bengal, India.

Explor. Anim. Med. Res., Vol.2, Issue - 1, 2012, p. 88-91 ISSN 2277- 470X

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107.0 mg/dl, Total Protein 5.6 gm/dl, Chloride89.6 mcg / l . The smear of ascitic fluidshowed presence of inflammatory and sheetsof reactive mesothelial cells.

Ultrasonography of whole abdomenrevealed overall gross ascites with a smallright sided pleural effusion. Hepatic veinswere apathy and dilated. Gall bladder was

distended and walls were thin, measured 2mm at the porta hepatis. Inferior vena cava(IVC) behind the liver was distended.

Fig.1: Irregular masses of enlargedhepatocytes with proliferation of reticularfibers showed pseudo-lobulation(10X)

Fig.2: The large hepatocytes showed fewmitotic figures with proliferation of reticularfibers there in. Some places the nuclei of fewhepatocytes showing hyper-chromasia withvesicular cytoplasm indicating irregular celldivision(40X).

Fig.3: Well developed proliferatinghepatocytes with large nuclei and few mitoticfigures (40X ) .

Fig.4: Periportal fibrosis and perivascularproliferation of bile duct, hepatic artery andportal vein. Necrosis of surroundinghepatocytes due to pressure of irregularlyscattered hepatocytes and reticularproliferation (10X).

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Exploratory Animal and Medical Research, Vol.2, Issue -1, July, 2012

Primarily considered ascites of inflammatoryor neoplastic etiology.

The dog was treated for last few monthswith several medicines without showing anyimprovement and that gradually became off-fed, reluctant to move, unfit for any workand finally died.

Postmortem examination revealed presenceof moderate amount of sero-sanguinous fluidin thoracic cavity and hyperamic thoracicwall in general. Lower part of trachea andbroncho-tracheal portion were anastomosedwith oesophagus, blood vessels, nerve alongwith surrounding tissues adhered with spine.Trachea was mild haemorrhegic. Lower partof trachea and broncho-tracheal portion wereanastomosed. Right lung was partlysolidified, suppurative and haemorrhegic.Left lung was pneumonic, cyanosed andconsolidated. Heart was hypertrophic andchambers were filled with clotted blood.Pericardium found congested. Diaphragmwas severely congested. Spleen was enlargedand anaemic. Liver was hypertrophic,cirrhotic along with perihepatitis. Stomachwas empty. Pancreas was atrophic andanaemic. Intestine was partly haemorrhegic.Mesenteric lymph nodes were enlarged andhaemorrhegic . Kidneys were hypertrophicand congestion in cortex. Urinary bladderwas thickened with scanty haemorrhages inmucosa. A large amount of dark strawcoloured ascitic fluid was revealed inabdominal cavity, which was collectedaseptically and Escherichia coli was isolated.

Hepato-cellular carcinoma was detected inhistopathological examination. Thearchitectural details showed irregular massesof enlarged hepatocytes with proliferationof reticular fibers given pseudo-lobulation

(Fig.1). The large hepatocytes showed fewmitotic figures with proliferation of reticularfibers there in. In some places the nuclei offew hepatocytes showed hyper-chromasiawith vesicular cytoplasm indicating irregularcell division (Fig.2). The section depicted awell developed proliferating hepatocytes withlarge nuclei and few mitotic figures (Fig.3).Periportal fibrosis and perivascularproliferation of bile duct, hepatic artery andportal vein were evident. The surroundinghepatocytes were almost necrosed due topressure of irregularly scattered hepatocytesand reticular proliferation(Fig.4). The livercells were anaplastic, arranged in trabecular oracinar pattern, mitosis and enlarged nucleicommonly seen, which corroborate with thefinding of Vegad (1995). The trabeculargrowth pattern was 2-8 cells wide layer oftumour cells, which showed similarities withthe findings of Mohan (1953). Tumour cellswere composed of nest and end to malignantappearing hepatocytes separated by dencebundle of collagen, which corroborate with thefindings of Cotran et al. (1994). Suppurativepneumonia and myocarditis were revealedduring histopathological examination of lungsand heart muscles respectively. Consideringall, it was finally concluded that the dogwas died due to multi-organ failure as aconsequence of hepato-cellular carcinoma.

ACKNOWLEDGEMENT

Authors are thankful to the Director ofAnimal Husbandry & Veterinary Services,West Bengal for providing necessary facilitiesfor this work and Central Industrial SecurityForce, Kolkata Port Trust, Kolkata forproviding materials .

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REFERENCES

Bertino JR.(1996). Encyclopedia ofCancer. Vol.II. Academica Press. Inc.California. USA. p.808-809.

Cotran RS, Kumar V and Robbins SL(1994). Robbin's Pathologic basis of disease.5th edn. Prism Book Pvt. Ltd. Bangalore.p.879-882.

Evans SM.(1987). The radiographicappearance of primary liver neoplasia in dogs.Vet Radiol. 28: 192-196.

Liptak JM, Dernell WS, Monnet E,Powers BE, Bachand AM, Kenney JG andWithrow SJ.(2004). Massive hepatocellularcarcinoma in dogs: 48 cases (1992-2002).J. Am. Vet. Med. Assoc. 225: 1225-1230.

Mohan H. ( 1953). Textbook of Pathology.2nd edn. Jay Pee Brothers. New Delhi. p.636-638.

Patnaik AK, Hurvitz AI and Lieberman

PH.(1980). Canine hepatic neoplasms : aclinicopathologic study. Vet Pathol. 17: 553-564.

Patnaik AK, Newman SJ and ScaseT.(2005). Canine hepatic neuroendocrinecarcinoma: an immuno-histochemical andelectron microscopic study. Vet Pathol. 42:140-146.

Sterczer A, Nemeth T, Mandoki M, GalfiP and Jakab C.(2011). A case of synchronoushepatocellular carcinoma and aortic bodychemodectoma in a dog - pathological casereport. Acta. Vet. Hung. 59(1): 113-121.

The Merck Veterinary Manual. (2010).10th edn. Merck Sharp & Dohme Corp. Merck& Co. Inc. USA.

Vegad JL .(1995). Textbook of VeterinaryGeneral Pathology. Vikash Publishing HousePvt. Ltd. New Delhi. p.284-285.

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